ADDENDUM TO IDSP REPORT NO. 10, REPORT TO THE WORKERS' COMPENSATION BOARD ON COR PULMONALE
APRIL 1996

OCCUPATIONAL DISEASE PANEL (INDUSTRIAL DISEASE STANDARDS PANEL)
ODP REPORT NO. 10A
TORONTO, ONTARIO

Occupational Disease Panel

When the Workers' Compensation Act was amended in 1985, the Occupational Disease Panel was created. The Panel was set-up to provide the Workers' Compensation Board with scientific and policy advice about the recognition and compensation of work-related diseases. The need for the Panel was identified by several individuals, including Professor Weiler, who studied the workers' compensation system and identified systemic under-compensation of disease claims.

The Panel is a decision-making body that is composed of representatives of the public and the scientific community and technical and professional persons. It has a small staff and is assisted by consultations with renowned experts in the areas of medicine and science.

The statute specifically sets out the following mandate (Workers' Compensation Act, R.S.O. 1990, c. W. 11, s.95):

95(8) It shall be the function of the Panel,

To assist with its work the Panel has a small staff of researchers, analysts and support people. In addition to its own staff, the Panel relies heavily on the advice of outside experts in science, medicine and law, as well as on input from interested parties.

Additional copies of this publication are available by writing:

Occupational Disease Panel
69 Yonge Street, Suite 1004
Toronto, Ontario M5E 1K3
(416) 327-4156

Panel Membership

Panel Staff

TABLE OF CONTENTS

Letter of transmittal
Panel Members
Panel Staff

Addendum to IDSP Report No. 10, Report to the Workers' Compensation Board on Cor Pulmonale: Background

The issue
The course of action

The Panel's Recommendations on the Implementation of Report No. 10.

References

Report of the Cor Pulmonale Committee to the ODP: Introduction

a. Definition of cor pulmonale
b. Diagnosis of cor pulmonale
c. Physical examination
d. Investigations of cor pulmonale

The Questions Posed to the Committee By the Board

1. What respiratory diseases are likely to lead to cor pulmonale?
2. How long does it take the respiratory disease(s) in question to progress to cor pulmonale?
3. Is it possible to distinguish work- and non-work-related cor pulmonale through medical assessments, and, if so, how?
4. What is the treatment for cor pulmonale apart from treatment of the underlying respiratory condition?

Committee Recommendations

Monitoring of Workers with Compensable Respiratory Disease for Pulmonary Hypertension and Cor Pulmonale

Bibliography

Appendix I.
Committee Members

Appendix II.
Pneumoconiosis Claims Review

Table 1.
Findings in the IDSP Report to the Workers' Compensation Board on Cor Pulmonale

Table 2.
Workers' Compensation Board Response to the IDSP Report on Cor Pulmonale

Table 3.
Methods of Investigating Pulmonary Hypertension and Cor Pulmonale

Table 4.
Respiratory Disorders Predisposing to Chronic Cor Pulmonale (5)

Table 5.
Therapeutic Goals and Treatment in Cor Pulmonale (5)

Table 6.
Guidelines for Chronic Oxygen Therapy

ADDENDUM TO IDSP REPORT NO. 10, REPORT TO THE WORKERS' COMPENSATION BOARD ON COR PULMONALE: BACKGROUND

IDSP Report No. 10, Report to the Workers' Compensation Board on Cor Pulmonale was issued in July 1992 and subsequently published in the Ontario Gazette,Vol.125-39,September 26,1992 (1).

The issue

During the 90 day period following the gazette notice, a total of five reviews were invited and received by the Board (2). An unsolicited letter was directed to the Chair of the Panel.

In general, there was support for the Panel's finding of probable connection between compensable respiratory disease and the development of cor pulmonale, and for the proposed strategy of monitoring workers for its development rather than establishing a presumption of work-relatedness. However there was a recognized need for standard criteria to aid in the diagnosis of cor pulmonale, and acknowledgement of the difficulty of attributing exclusive cause of the cor pulmonale to the compensated lung condition. The correlation between the severity of the respiratory disease and the likelihood of the development of cor pulmonale was stressed by several authors.

The course of action

It has always been the intention of the Members of the Occupational Disease Panel to provide advice to the Board that is scientifically accurate, in accordance with the current legislation, and practical in its implementation.

In order to address some of the points raised in the reviews of the Panel's initial report and in informal conversations with Board staff, the Chair of the Panel, in a letter to the Senior Vice-President of Strategic Policy, suggested that a special ODP/WCB joint committee be established (3).

The Board agreed and the Cor Pulmonale Committee was struck, composed of the following members:

The mandate of the Committee was to "develop guidelines to assist adjudicators and physicians in the possible early identification of cor pulmonale".

The Board formulated additional questions of its own to be addressed by the Committee: (4)

1. What respiratory diseases are likely to lead to cor pulmonale?
2. How long does it take the respiratory disease(s) in question to progress to cor pulmonale?
3. Is it possible to distinguish work and non-work-related cor pulmonale through medical assessments, and, if so, how?
4. What is the treatment for cor pulmonale apart from treatment of the underlying respiratory condition?

The Panel was pleased to receive the final report of the Cor Pulmonale Committee at the ODP meeting of December 6-7, 1995. It is attached as the "Report of the Cor Pulmonale Committee to the ODP (page 13)" and addresses the issues surrounding standard diagnostic criteria and the above questions.

The Cor Pulmonale Committee devoted considerable time to exploring various diagnostic means of detecting cor pulmonale. While the Panel would not presume to advise medical practitioners as to their choice of procedures, it encourages the Board to share the Committee's document with treating physicians where appropriate and to authorize the recommended testing to aid in the diagnosis where such information is lacking from a file.

The Panel's Recommendations on the Implementation of Report No. 10.

The Panel is grateful for the diligent work of the joint ODP/WCB Committee and feels that the Committee's Report is invaluable in facilitating the sensible implementation of the Panel's initial recommendations.

The Panel is prepared to accept the medical consensus that cor pulmonale would normally occur only late in the course of severe disease. However, it also recognizes, as discussed in IDSP Report No.11 (5), that respiratory disability or impairment can result from several concurrent diseases, of which one or more may not be work-related, due to the cumulative impact on lung function.

Keeping the conclusions of the Committee in mind the Panel:

1. Reiterates its finding of probable connection between compensable respiratory disease and the development of cor pulmonale.

As outlined in the original report, the historical concern, which was also acknowledged by the Chair of the WCB in his original letter of referral, has been that some workers suffering from compensated respiratory disease can and do develop cor pulmonale which worsens their condition during life and may ultimately be listed as their cause of death. Evidence from various sources cited in the ODP's report to the WCB and including the Royal Commission on Asbestos, indicates that such worsening disability and death frequently go unrecognized as related to their compensable condition and hence uncompensated.

In a worker who is entitled to compensation for a sufficiently severe respiratory impairment, the development of cor pulmonale is intimately related to the compensable disease. The issue is whether and when, in such cases, cor pulmonale should attract additional compensation during life and dependency benefits upon death, even in the presence of concomitant non-work-related disease. The issue is not whether such workers die prematurely from the condition, or whether such workers die more frequently from the condition, than the general population.

2. The Panel recommends:

Original recommendation 1a & 1b:⁽²⁾

Bill 162, which came into force in full on January 2, 1990, altered the Board's system of compensating workers with permanent impairments. The previous compensation method was based on a clinical rating schedule with compensation levels calculated solely on the basis of degree of physical impairment. Some respiratory claims had scheduled follow-up, as described in Appendix II of the Committee's Report.

Bill 162 instituted a dual award system, with one award, the "non-economic loss" (NEL), intended to compensate for any permanent impairment, and the second, the "future economic loss"(FEL), intended to compensate the injured worker for reduced earning potential. Permanently impaired workers may be eligible for NEL or NEL and FEL awards, the NEL award being comparable to the pre-Bill 162 award for

permanent disability. Entitlement for a FEL award is considered if the worker has received temporary total disability benefits for 12 continuous months.

Hence, the implementation of the monitoring recommendation is complicated by the existence of differing categories of claims:

• Pre-Bill 162 workers with a pneumoconiosis claim who are already being followed as outlined in Appendix II of the Committee's Report.
• Pre-Bill 162 workers who were not recommended for regular follow-up
• Post-Bill 162 workers who have received a first Non-Economic Loss (NEL) assessment
• Post-Bill 162 workers who have yet to receive a first NEL assessment.

Under the current system (post-Bill 162) there is no mechanism for regular follow-up to reassess the degree of impairment after the NEL assessment except at the initiation of the worker. Therefore, the Board will need to develop guidelines for monitoring post-Bill 162 workers who qualify under the cor pulmonale policy to ensure equity between pre- and post-Bill 162 claims.

The Panel suggests that such screening could occur at the following intervals:

Pre-Bill 162 Workers
. with a pneumoconiosis claim . with an accepted respiratory claim which does not require ongoing monitoring	at least every two years at least every two years
Post-Bill 162 Workers
. before NEL award . with a NEL award	prior to assessment at least every two years

This screening should facilitate implementation of recommendation 1b (please see p.6). The medical findings should be provided to the worker's treating physician so that proper treatment can be enhanced. Proper diagnosis of the existence of cor pulmonale should result in fairer compensation for workers suffering from multiple impairments.

Original recommendation 2a & 2b.

Adjudication of such claims involving cor pulmonale should proceed on a case-by-case basis. The testing that has been recommended by the Committee should help correct the adjudicatory problems surrounding cause of death in these cases.

The Panel accepts the conclusion of the Cor Pulmonale Committee that it is not possible to distinguish between work-related and non-work-related cor pulmonale. The Panel is also guided by Section 3(4) of the Workers' Compensation Act:

REFERENCES

* Due to copyright restrictions, references may not be reproduced by photocopying. All references are available at the WCB library.

1. Industrial Disease Standards Panel. Report to the Worker's Compensation Board on Cor Pulmonale. Toronto: Industrial Disease Standards Panel, July 1992.

2. Various. [Report Containing Submissions to the Workers' Compensation Board on the IDSP Report to the Workers' Compensation Board on Cor Pulmonale]. Compiled January, 1993.

3. Carlan,N. Re: Cor Pulmonale. [Letter to L. Jolley]. January 13, 1993.

4. Jolley,L. [Letter to N. Carlan]. June 15, 1993.

5. Industrial Disease Standards Panel. Report to the Workers' Compensation Board on Respiratory Complications among Workers receiving Compensation for Non-malignant Respiratory Disease. Toronto: Industrial Disease Standards Panel. March, 1993.

6. American Medical Association. Guides to the Evaluation of Permanent Impairment. 3rd.ed. Chicago: American Medical Association, 1990.

7. Workers' Compensation Act. Revised Statutes of Ontario, 1990. Chap.539, Sec.3(4).

REPORT OF THE COR PULMONALE
COMMITTEE TO THE ODP:

INTRODUCTION

In July of 1992 the Occupational Disease Panel (ODP) - formerly the Industrial Disease Standards Panel - issued a Report to the Workers' Compensation Board on Cor Pulmonale(1). The recommendations of the IDSP on cor pulmonale are listed in Table 1. After publication of the IDSP Report on Cor Pulmonale in the Ontario Gazette, the Chair of the Panel proposed the formation of a joint Panel-Board committee, with perhaps an independent expert participating, to "develop guidelines to assist adjudicators and physicians in the possible early identification of cor pulmonale" (2). The Workers' Compensation Board (WCB) subsequently agreed and presented to the ODP additional questions about cor pulmonale of occupational origin. These additional questions are listed in Table 2. The committee (Appendix I) composed of an ODP Panel Member, a member of the academic community and two from the WCB, met three times over the ensuing two years, reviewed extensive material both individually and collectively and revised several draft documents. This report to the ODP represents a Committee consensus. The Committee's report should be of help in the implementation of the recommendations of the original IDSP Report on Cor Pulmonale, by providing advice as to methods for diagnosing and monitoring cor pulmonale and its precursor condition of pulmonary hypertension. The report also attempts to address the questions raised by the Board as outlined in Table 2.

a. Definition of cor pulmonale

Cor pulmonale is defined as hypertrophy of the right ventricle that results from diseases affecting the function and structure of the lung, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart, or are from congenital heart disease (3). However, it has been proposed that the term cor pulmonale should be abandoned in favour of a more precise definition that is based on objective evidence of right ventricular hypertrophy, enlargement, functional abnormality or failure (4). As MacNee points out, the problem of defining cor pulmonale produces considerable difficulties when comparing patients from different studies (4).

This Committee report uses the term cor pulmonale as defined according to the World Health Organization (3).

b. Diagnosis of cor pulmonale

Cor pulmonale is difficult to diagnose on clinical grounds because signs and symptoms are late and non-specific (5). The symptoms may include dyspnea, orthopnea, fatigue and dizziness. When the right ventricle fails the clinician may measure weight gain, abdominal distention and peripheral edema. The clinical criteria are considered very insensitive and are present late in the disease course.

The effect of pulmonary hypertension, right ventricular enlargement and/or right ventricular hypertrophy on the left ventricle is not clear. Usually left ventricular function is not affected. Although the conventional view is that the two ventricles are independent they are in fact part of the same muscle bundle and pericardium, share a common wall, and are enclosed within the pericardium. Increased pressure in the right ventricle may displace the septum into the left ventricle encroaching on its lumen and modifying left ventricular volume and pressure.

The most common cause of right ventricular failure is left ventricular failure. If there is significant left ventricular failure present it is considered to be the cause of the right ventricular failure, rather than the effect. If biventricular failure is detected along with the presence of significant respiratory disease (Class 3-4 AMA guidelines) one has to determine a relative contribution of the lung disease in causing the right ventricular failure to ensure appropriate treatment.

c. Physical examination

On examination there may be a parasternal lift indicating right ventricular hypertrophy, an increased P₂ component of S₂ and a right ventricular S₄. When the right ventricle fails there are additional findings such as jugulovenous distension, hepatojugular reflux, a right ventricular S₃ gallop, pulmonary and tricuspid regurgitant murmurs, hepatomegaly, ascites and peripheral edema. These latter findings are of advanced disease (6).

d. Investigations of cor pulmonale

The investigation to determine the presence of right ventricular hypertrophy and pulmonary arterial hypertension should be simple, not expensive, non-invasive and therefore repeatable without harm to the patient. The tests should be sensitive and specific enough and should be available in most hospitals.

The gold standard for measuring pulmonary arterial hypertension is cardiac catheterization. However, cardiac catheterization is invasive, risky, and not easily repeated for follow-up. It also requires specially trained personnel and laboratory back-up. Magnetic resonance imaging (MRI) measures other evidence of pulmonary artery hypertension and cor pulmonale, such as right ventricular volume and right ventricular wall hypertrophy. However, MRIs are costly and not easily available.

Table 3 lists a number of investigations which can be used to assess the severity of underlying pulmonary disease along with information regarding right ventricular function and pulmonary arterial pressure. These test measurements should correlate well with measurements of right pulmonary arterial blood pressure or right ventricular systolic pressure if they are to be of value.

Many of the tests listed in this table either lack sensitivity or specificity (e.g. chest x-ray, ECG) or are not easily available (First Pass Radionuclide Angiography, MRI, Radioactive Thallium). Although cor pulmonale has at its root hypoxemia and reduced pulmonary vascular bed, resting arterial blood gas values may not reflect risk. Arterial blood gases may decrease with exercise and sleep and these decreases can be detected by monitoring of arterial blood gases continuously for 24 hours.

After thoroughly reviewing the spectrum of procedures available, the Committee is of the unanimous opinion that two-dimensional (2D) echocardiography with Doppler flow study is the most useful and readily available measurement of right ventricular systolic pressure and right ventricular size.

THE QUESTIONS POSED TO THE COMMITTEE BY THE BOARD

1. What respiratory diseases are likely to lead to cor pulmonale?

Cor pulmonale can be considered acute or chronic. This report excludes consideration of acute causes such as pulmonary embolism.

The respiratory disorders predisposing to chronic cor pulmonale are tabulated according to Fishman (7) in Table 4. Amongst all conditions causing chronic cor pulmonale, the most common is obstructive lung disease.

According to the Committee members from the WCB, the common occupational conditions causing cor pulmonale, in descending order of frequency, are the pneumonoconioses, chronic obstructive lung disease and scleroderma.

More than one disorder may be present at the same time. A diffuse pulmonary interstitial disease and chronic obstructive lung disease may exist at the same time. Obstructive apnea syndromes may lead to a nocturnal hypoxia which can exacerbate any underlying problems with hypoxemia. In addition to this, intercurrent infections can lead to a transient hypoxemia and likewise, exacerbate underlying problems.

Early in its deliberations, the Committee decided to expand this question to include "What severity of chronic respiratory diseases are likely to lead to cor pulmonale?"

A 1984 review found that an increased likelihood of pulmonary hypertension occurred in patients with severe respiratory obstruction (FEV_1.0 < 70% and DLCO <70% predicted) or severe respiratory restriction (FVC <40% and DLCO <60% predicted) (8). Arterial oxygen saturation <85% was also an indicator of possible pulmonary hypertension.

More recently, Shivkumar (9) has correlated pulmonary function data with right ventricular wall thickness, right ventricular dilatation and pulmonary hypertension in patients with a pure restrictive ventilatory impairment, using 2D and M-mode echocardiography with pulsed Doppler ultrasound. Shivkumar reports normal pulmonary artery pressure in patients with a forced vital capacity greater than 60% predicted. This would translate into the respiratory impairment classification of the American Medical Association Guide to the Evaluation of Permanent Impairment of a normal pulmonary artery pressure in patients with a Class 1 or Class 2 impairment (less than 25% impairment of the whole body)(10).

2. How long does it take the respiratory disease(s) in question to progress to cor pulmonale?

There is a general lack of reports to provide evidence about the time for chronic respiratory disease to progress to cor pulmonale. There is unclear progression of the respiratory disease to the onset of pulmonary hypertension and from pulmonary hypertension to cor pulmonale.

The hemodynamics of early cor pulmonale are characterized by elevations in pulmonary vascular resistance and elevations in mean pulmonary artery pressure. Sustained increase in the pulmonary vascular resistance is caused by hypoxemia-induced vasoconstriction and/or obliteration of the small pulmonary arteries and arterioles. This results in pulmonary hypertension. Sustained hypoxemia (partial pressure of oxygen in arterial blood (PaO₂) of 55 mm Hg or less, or arterial oxygen saturation (SaO₂) of 88 % or less (6) causes anatomic changes in the vascular bed that are generally irreversible. If arterial oxygen saturation is less than 85%, then 93% of COLD patients and 100% of patients with fibrosing alveolitis have pulmonary hypertension (5). As pulmonary arterial pressure increases and the workload of the right ventricle increases, right ventricular hypertrophy develops (cor pulmonale).

Hence, the primary event preceding the development of cor pulmonale is pulmonary hypertension. Pulmonary hypertension is considered to be a precursor condition in the development of cor pulmonale. It is clear that follow-up is required once pulmonary hypertension is diagnosed to watch for signs of right ventricular failure. However, the benefit of early treatment of pulmonary hypertension with early detection has not been demonstrated.

Some studies show shorter survival in patients with chronic obstructive pulmonary disease and high pulmonary artery pressure compared to those with lower pulmonary artery pressure (11).

Some information comes from a report of progression of pulmonary artery pressure at <1mm Hg per year in patients with chronic obstructive lung disease (COLD)(12). Another study found that untreated pulmonary hypertension in patients with chronic obstructive lung disease progressed an average of 3mm Hg per year (11).

Jandova and colleagues found that patients with silicosis and pulmonary hypertension had a mean survival of 7.6 years (13,14). Patients with silicosis, but without pulmonary hypertension, had an average survival of 11.3 years.

Widimsky, who was involved in the WHO studies of non-invasive diagnosis of pulmonary hypertension is of the opinion that it may exist for a considerable time before right ventricular hypertrophy develops (5).

Investigators in studies of pulmonary artery pressure data tend to select patients with suspected pulmonary hypertension before cardiac catheterization. Most studies do not provide a time from the absence of pulmonary hypertension to the detection of enlargement of the right ventricle.

Thus in summary, patients with diagnosed pulmonary hypertension should be followed for development of cor pulmonale. However, available studies do not provide information on which to base an estimate of the time for chronic respiratory disease(s) to progress to cor pulmonale.

3. Is it possible to distinguish work- and non-work-related cor pulmonale through medical assessments, and, if so, how?

As Fishman notes, after age 50 cor pulmonale is the most common cardiac disorder except for coronary and hypertensive heart disease and most of these instances (of cor pulmonale) are secondary to obstructive disease of the airway and subsequent pulmonary hypertension that follows. Cor pulmonale is found in about half of COLD patients at autopsy (7). COLD of occupational origin (6, 15) is difficult to measure in the presence of non-occupational confounding exposure to tobacco smoke: however, it is likely that COLD of occupational origin affects both smokers and nonsmokers (16).

While monitoring can provide evidence to establish the existence of cor pulmonale, monitoring will not in itself provide evidence to distinguish between work and non-work-related disease.

Chronic cor pulmonale does not vary with the cause. Thus, medical assessments of the heart and pulmonary vessels cannot identify the cause of the abnormalities. The likelihood of cor pulmonale developing depends on the severity of the underlying chronic respiratory condition. Any restrictive or obstructive pulmonary disease of sufficient severity can lead to chronic cor pulmonale. Whether the pre-existing respiratory condition is work-related will already have been determined by the Board, as the focus of the original IDSP Report on Cor Pulmonale was on workers already receiving permanent disability awards for respiratory impairment.

4. What is the treatment for cor pulmonale apart from treatment of the underlying respiratory condition?

The reader is referred to Table 5. Not included in this list is lung transplantation, which, although an heroic measure, has been used successfully. The diagnosis of cor pulmonale indicates poor prognosis. It is uncertain whether the impairment of the right ventricle is a predictor of mortality or whether cor pulmonale merely parallels the severe ventilatory abnormalities seen in these patients. It is uncertain then that management of cor pulmonale is any more than management of the severe underlying respiratory disease. Since hypoxemia is a root cause of pulmonary arterial hypertension, treatment of the underlying condition which has led to the hypoxia, along with supportive measures to correct respiratory infection, arrhythmia, features of fluid overload, etc. is essential.

Oxygen therapy for pulmonary hypertension and cor pulmonale, especially in obstructive lung disease, is a standard treatment (17,18). Oxygen treatment relieves hypoxic vasoconstriction in patients with cor

pulmonale and is analogous to the use of vasodilators in patients with hypertension and left ventricular hypertrophy.

The majority of patients who are chronically hypoxic should receive a minimum of 18 hours of oxygen therapy a day (see Table 6). Patients who have early nocturnal oxygen desaturation are candidates for overnight rather than continuous (18 to 24 hours a day) oxygen supplementation. Other potential causes of hypoxia such as sleep apnea should be reviewed and corrected if possible.

COMMITTEE RECOMMENDATIONS

Although the Committee's initial mandate was to recommend methods to diagnose chronic cor pulmonale,the Committee of necessity, expanded its mandate to include not just cor pulmonale, but the recognized precursor condition of pulmonary artery hypertension.

The Committee reviewed information about the available non-invasive investigations for pulmonary artery hypertension and cor pulmonale. It also reviewed which workers with compensable chronic respiratory diseases would be at risk of developing pulmonary artery hypertension and cor pulmonale. As a result of those deliberations, the Committee suggests the following to the Occupational Disease Panel:

MONITORING OF WORKERS WITH COMPENSABLE RESPIRATORY DISEASE FOR PULMONARY HYPERTENSION AND COR PULMONALE

WHO?

Screen all workers with a compensable respiratory disease with a respiratory disability or impairment equivalent to Class 3 or 4 respiratory impairment according to the AMA Guides to the Evaluation of Permanent Impairment.

WHEN?

For those workers being followed for a pneumoconiosis claim, this may be most conveniently done at the recommended follow-up as prescribed in Appendix II.

If a pre-bill 162 claim was not recommended for regular follow-up, then every two years.

If post-bill 162, the screening could most conveniently be done prior to the first Non-economic loss (NEL) assessment.

HOW?

2-dimensional echocardiogram with Doppler flow study. It is assumed that some additional testing will be available on file as well, such as simple spirometry, pulmonary function tests, ECG, chest x-ray and/or arterial blood gases.

The AMA Guides do not contain specific guidelines for assessing impairment due to cor pulmonale. The AMA Guides do indicate that where there are two or more impairments, the Combined Values Chart of the AMA Guides should be used for combining the impairments. The AMA Guide indicates that "the physician should look for evidence of cor pulmonale which may be associated with conditions such as chronic bronchitis and emphysema and with chronic diffuse interstitial disease of sufficient severity. The physician should determine impairment of the cardiovascular system which should be combined with the impairment rating for pulmonary diseases according to the Combined Values Chart".

It is apparent that guidelines will have to be developed for evaluating cor pulmonale that can be applied to both pre and post-Bill 162 claims. For post-Bill 162 claims, the impairment for cor pulmonale should be combined with other impairments using the Combined Values Chart as described above.

BIBLIOGRAPHY

* Due to copyright restrictions, references may not be reproduced by photocopying. All references are available at the WCB library.

1. Industrial Disease Standards Panel. Report to the Workers' Compensation Board on Cor Pulmonale. July, 1992.

2. Carlan, N. Re: Cor Pulmonale. [Letter to L.Jolley]. January 13, 1993.

3. World Health Organization. Chronic Cor Pulmonale: Report of the World Health Organization Expert Committee. Circulation. Vol.XXVII (April, 1963).

4. D. MacNee, W. Pathophysiology of cor pulmonale in chronic obstructive pulmonary disease. American Journal of Respiratory and Critical Care Medicine. (1994). p.150, 833-852.

5. Widimsky, J. Noninvasive diagnosis of pulmonary hypertension in chronic lung disease. Progress in Respiratory Research. Vol.20 (1985). p.69-75.

6. Murphy, M.L.; Bone, R.C. Cor pulmonale in chronic bronchitis and emphysema. Mount Kisco, NY: Futura, 1984.

7. Fishman, A.P. Cor pulmonale. In: Wilson, J.D.;Braunwald, E., eds. Harrison's Principles of Internal Medicine. 11th ed. Toronto: McGraw-Hill, 1987. p.993-998.

8. Chappell, T.R. Pulmonary function and exercise testing. In: Lubin, L.J., ed. Pulmonary Heart Disease. Boston: Martinus Nijhoff, 1984.

9. Shivkumar, K.; Ravi, K.; et al. Right ventricular wall thickening and Doppler evidence of pulmonary hypertension in patients with pure restrictive ventilatory impairment. Chest. Vol.106(1994). p.1649-1653.

10. American Medical Association. Guides to the Evaluation of permanent Impairment. 3rd.ed. Chicago: American medical Association, 1990.

11. McFadden, R.E.; Braunwald, E. Cor pulmonale. In: Braunwald, E., ed. Heart Disease. 4th ed. New York: Saunders, 1992. p. 1592-1593.

12. Weitzenblum, E.; Sautegau, A.; et al. Long-term course of pulmonary artery pressure in chronic obstructive pulmonary disease. American Review of Respiratory Diseases. Vol.130(1984). p.993-998.

13. Jandova, R.; Widimsky, J.; et al. Long-term prognosis of pulmonary hypertension in silicosis. Cor vasa. Vol.22(1980). p.221-237.

14. Jandova, R.; Widimsky, J. Long-term prognosis of pulmonary hypertension in silicosis. Bulletin de Physio-pathologie Respiratoire. Vol.16(1980). p.128-131.

15. S. Sherman. Cor pulmonale. Postgraduate Medicine. Vol.9I, no.6 (1992). p.227-236.

16. Oxman, D.A.; Muir, D.C.F.; et al. Occupational dust exposure and chronic obstructive pulmonary disease. A systematic overview of the evidence. American Review of Respiratory Diseases. Vol148(1993). P.38-48.

17. Medical Research Council Working Party. Long-term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema. Lancet. Vol.1(1981). p. 682-5.

18. Nocturnal Oxygen Therapy Trial Group. Continuous or nocturnal oxygen therapy in hypoxemic chronic obstructive lung disease. A clinical trial. Annals of Internal Medicine. Vol.93(1980). p. 391-8.

APPENDIX I.
COMMITTEE MEMBERS

APPENDIX II.
PNEUMOCONIOSIS CLAIMS REVIEW

ASBESTOS EXPOSURE
No asbestos-related changes	No follow-up
Pleural changes only	4 years*
Changes consistent with asbestosis**
Unstable	1 year
Stable continued exposure	2 years
Stable no exposure	3 years

* Follow-up limited to twice at 4 year intervals up to 8 after no longer exposed.

** Follow-up continues indefinitely for lifetime.

TABLE 1.

FINDINGS IN THE IDSP REPORT TO THE WORKERS' COMPENSATION BOARD ON COR PULMONALE

TABLE 2.

WORKERS' COMPENSATION BOARD RESPONSE TO THE IDSP REPORT ON COR PULMONALE

TABLE 3.

METHODS OF INVESTIGATING PULMONARY HYPERTENSION AND COR PULMONALE

TABLE 4.

RESPIRATORY DISORDERS PREDISPOSING TO CHRONIC COR PULMONALE (5)

TABLE 5.

THERAPEUTIC GOALS AND TREATMENT IN COR PULMONALE(5)

TABLE 6.

GUIDELINES FOR CHRONIC OXYGEN THERAPY

May 10, 1996

Mr. Brock Smith
Acting President and CEO
Workers' Compensation Board
200 Front Street West, 18th Floor
Toronto, Ontario
M5V 3J1

Dear Mr. Smith:

I enclose a copy of the Panel's "ADDENDUM TO IDSP REPORT NO. 10, REPORT TO THE WORKERS' COMPENSATION BOARD ON COR PULMONALE".

This Report is the result of a consultation process between nominees from both the Workers' Compensation Board and the Occupational Disease Panel. It is our hope that we will be able to collaborate in the future to best serve our mutual clients.

I would be pleased to discuss the Report with you at your convenience.

Sincerely,

Nicolette Carlan
Chair

Endnotes

1. The term total in this recomendation is inclusive of non-compensable respiratory diseases.

2. The Panel regrets the confusion caused by the inadvertant use of the word "bi-annual­ in its initial recommendation. Obviously, that is too frequent a follow-up, the original intention being "biennial" or every two years for those pre-Bill 162 workers who are not recommended for regular review.